Hypo and Hyper Nat Re Mia

8/2/2019 Hypo and Hyper Nat Re Mia

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Presenter:Dr.Nazma.N.RDate: 23/08/2011

Time:9:00 amVenue: seminar hall, INU


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50%60%


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ECF ICF


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1/3rd

plasma

2/3rdinterstitium

ECF


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ECF ICF

Na+

Cl-

HCO3-

K+ Organic phosphate

esters like ATP,creatine phosphate,

phospholipids

Solute distribution


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Intake

Excretion


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Osmotic

threshold

295

mosm/kg

Osmoreceptors in

anterolateral

hypothalamus

Thirst


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Osmotic

threshold 280-

290 mosm/kg

AVP secretionV2 receptors in

collecting duct


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Regulation by:-

Kidney through interaction of neurohumoralmechanisms including

1. RAAS2. Sympathetic nervous system3. ANP4. BNP

Effective circulating volume(ECV)


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Tubular sodium

reabsorption

2/3rdsin PCT

25-30%

in TALH

5% inDCT

[Main regulatory step]


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[Na+ ] < 135 mmol/L Usually hypotonic, but can be isotonic or

hypertonic

excess of body water in relation to bodysodium

Most common electrolyte abnormality


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1% -----acute symtomatic 4%------acute asymptomatic

75-80%--chronic asymptomatic

1-2%----hospitalised patients


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Old age DM

CKD

Surgery Pulmonary infection

Diuretics

Antibiotics

Opioid analgesics


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Predicts mortality in post MI, CHF, cirrhosispts

In critically ill pts, Na


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Acute :-

1. Mild [130-135] often asymptomatic

2. [125-130]

fatigue, malaise, nausea,unsteadiness

3. [115-120] headache, restlessness,lethargy, obtundation, seizures, coma,

brainstem herniation, respiratory arrest,death


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Chronic:-

Brain undergoes osmotic adaptation bytransporting

1. Na, K, Cl into ECF

2. Organic solutes [osmolytes] like glutamine,taurine, myoinositol


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Hyponatremia

Hyperosmolar Isoosmolar Hypoosmolar

Hypovolemic Isovolemic Hypervolemic


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Hypervolemia

Heart failure

Hepatic cirrhosis

Nephrotic

syndrome

Renal

insufficiency

Euvolemia

SIADH

Hypothyroidism

Adrenal

insufficiency

Hypovolemia

Extrarenal Na

loss if urine Na20mmol/L


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Simultaneous loss of solute &

water from ECF

Reduced ECV

Non-osmolar stimulation of

AVP release

Reduced free water loss


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Critically ill pts with intracranial injury,neurosurgery, glioma, TB or Ca. meningitis

Increased sympathetic activity, ANP, BNP

Natriuresis & volume depletion

AVP induced water retention


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Inappropriately high urine osmolality

High urine Na [>40 mEq/L] High serum AVP

DD:

SIADH typically euvolemic/ mild volumeexpansion in contrast to hypovolemia in CSW


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SIADH Endocrinopathies

Pregnancy


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Criteria Major :-

1. Reduced ECF osmolality [100]

3. Clinical hypovolemia4. Urine Na > 40mEq/L

5. Absence of hypothyroidism, hypocortisolism &diuretic use

6. Normal S.creatinine7. Normal acid-base & K balances

8. Low S. urea & uric acid levels


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Minor1. Abnormal water load test

2. High plasma AVP relative to plasmaosmolality

3. No significant correction of plasma Na withvolume expansion but improvement afterfluid restriction


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Adrenal insufficiency

Low CO & BP Na wasting & low ECF volume

Increased release of AVP


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Hypothyroidism

Low CO Inability to max. suppress AVP

Increased AVP


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Pregnancy

High HCG downward reset osmostat

Mild asymptomatic hyponatremia


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CHF

Low CO, BP Carotid baroreceptors

AVP releaseRenal hypoperfusion

Activation of RAAS,

sympathetic system

Na & water retention


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Cirrhosis

Splanchnic & systemic vasodilatation

Reduced ECF

Non-osmotic release of AVP


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Abnormal thirst stimulus

Excess free water intake

Psychiatric illnesses, antipsychoticmedications, sarcoidosis, MDMA [ecstacy]


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Poor dietary intake of solute:-Beer potomania, malnutrition


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Hyperglycemia Mannitol, sorbitol

2.4 mmol/L of Na fall for every 5.6 mmol/L ofglucose [1.6-2 mEq/L of Na/100mg/dl ofglucose]


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Accumulation of isotonic non-sodiumcontaining fluid in extracellular space [eg.,bladder irrigation with glycine] or

Hyperproteinemia, hyperlipidemia

[ pseudohyponatremia ]


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Goals

To increase plasma sodium by reducing waterintake and increasing water loss

To correct underlying cause


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Mild asymptomatic hyponatremia:-requires no treatment

Asymptomatic hyponatremia associated withhypovolemia:-sodium repletion with isotonic saline

Hyponatremia with hypervolemia:-1. Water restriction2. Sodium restriction3. Loop diuretics

4. Potassium deficit correction


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Hyponatremia associated with primarypolydipsia, renal failure and SIADH :-

water restriction

Vasopressin antagonists like conivaptan areused for selective treatment of euvolemic andhypervolemic hyponatremic patients.


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Depends on:-

Presence or absence of neurologicaldysfunction

Rapidity of onset

Magnitude of fall in sodium


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Asymptomatic :No > 0.5-1 mmol/L/h


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Quantity of sodium requiredfor correction

Sodiumdeficit TBW


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[Na+] > 145 mmol/L Hyperosmolar Relative deficit of body water in relation to

body Na content

1% of hospitalised pts

Causes:-

Primary sodium gain or

Water deficit(majority of times)Most common--iatrogenic


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Risk factors:- Old age

DM

Prior brain surgery

Diuretics

Altered mental status


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Na> 150 mmol/L increases mortality esp., inhospital acquired cases


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Initialnon-specific symptoms Later hyperreflexia, seizures, coma

[158-160 mmol/L]


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Hypernatremia

Hypovolemic

Min volume of

max concentrated

urine

Hypervolemic

Administration of

hypertonic NaCl

or NaHco3

Extra RenalWater loss

Renal waterloss

Yes No


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Urine osmole

excretion>750

mosm/d

Osmotic

diuresis

Diuretics

Renal osmolality

in response to

desmopressin

Rises

Central DI

Unchanged

Nephrogenic DI

Yes

No


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Goals1. To stop ongoing water loss by treating

underlying cause

2. To correct water deficit


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Water deficit

Plasma sodium-140

________________140

TBW


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Slowly over atleast 48-72 hrs 0.5 mmol/L/h

No > 12 mmol/L/24 hrs


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Safest is oral Alternate-5%D or 0.45% saline


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Intranasal desmopressin Low salt diet in combination with thiazide

diuretics to reduce urine output

Drugs which stimulate AVP secretion orenhance its action:-

chlorpropamide, clofibrate, carbamazepine,NSAIDs


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Treat underlying disorder Low salt diet with thiazides

NSAIDs-potentiate AVP action


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Thiazides induce mild volume

depletion

Increases proximal absorption of

salt and water

Decreased delivery of the filtrate

to the site of action of AVP


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Other causes of NDI:- Lithium toxicity--------------------

Sodium channel antagonist- Amiloride

Hypokalemia

Hypercalcemia


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Hypo and Hyper Nat Re Mia